Glial cells are thought to play a passive role in neuronal and synaptic activity. The products of neuronal firing, potassium and neurotransmitters, released from the neuron, must be controlled so that normal neuronal and synaptic function can proceed. Glial cells are believed to take up potassium and neurotransmitters required from the neuron. Successful glial control of K+ (i.e., spatial buffering) required a predominant permeability to K+ and the current dogma states that only potassium directly alters the membrane potential of glial cells. However, over the past seven years, three laboratories working with different glial preparations, have found that a putative neurotransmitter, L-glutamate, directly depolarizes the membrane potential of glial cells. These findings raise the possibility that glial cells at the synapse respond electrically to neurotransmitters released from the presynaptic neurons and that information is transferred between neuronal and glial cells. It is likely that our current beliefs concerning spatial buffering, synaptic and ephaptic transmission will have to be re-evaluated. In addition, models of disease processes thought to involve neurotransmitters (e.g. epilepsy, depression) may have to be modified to include a direct role of glial cells. The goal of this study is to determine if the L-glutamate depolarization in astrocytes (a type of glial cell) in primary cell culture involves an electrogenic mechanism (perhaps the L-glutamate uptake system) or a receptor mediated ion channel opening. Electrophysilogical techniques such as intracellular recording and patch clamp will be used in conjunction with radio-labelled tracer studies.